Ameliorative Effect of Epigallocatechin Gallate on Cardiac Hypertrophy and Fibrosis in Aged Rats

Abstract

The objective of the present study is to evaluate the effect of epigallocatechin gallate (EGCG) on aging-mediated cardiac hypertrophy, fibrosis, and apoptosis. The Wistar albino rats were divided into 4 groups (n = 18). Group I: young (3 months), group II: aged (24-26 months), group III: aged + EGCG (200 mg/kg for 30 days), and group IV: young + EGCG. At the end of 30 days, EGCG administration to the aged animals showed significant (P < 0.001) reduction of low-density lipoprotein, very low-density lipoprotein, triglyceride, total cholesterol with concomitant increase of high-density lipoprotein (P < 0.001) when compared with aged rats. Increased (P < 0.001) heart volume, weight with concomitant increase of left ventricular wall thickness, and reduced ventricular cavity were observed in aged rats supplemented with EGCG compared with aged animals. Histology and histomorphometry study of aged animals treated with EGCG showed marked increases in the diameter and volume of cardiomyocytes with concomitant reduction of numerical density when compared with aged animals. Reduced reactive oxygen species (P < 0.001) production with association of increased antioxidant defense system (P < 0.001) in aged hearts supplemented with EGCG when compared with aged animals. TUNEL staining and fibrosis showed a marked increase in apoptotic cell death (P < 0.001) and collagen deposition (P < 0.001) in aged animals treated with EGCG when compared with aged animals. Aged animals treated with EGCG showed a marked increase in protein expression of TGFβ, TNFα, and nuclear factor kappa B (NF-κB) and significant (P < 0.001) alteration in the gene expression of TGFβ, TNFα, NF-κB, α-SMA, and Nrf2 when compared with aged animals. Taken together, it is evident that EGCG may potentially inhibit aging-induced cardiac hypertrophy, fibrosis, and apoptosis, thereby preserving cardiac function. The proposed mechanism would be inhibition of reactive oxygen species-dependent activation of TGFβ1, TNFα, and NF-κB signaling pathway. Hence, the present study suggests that EGCG can be useful to fight against aging-induced cardiac hypertrophy, fibrosis, and apoptosis.

(-)-Epicatechin Inhibits Cardiac Fibrosis via SIRT1/AKT/GSK3β Pathway

“…Furthermore, EPI protected myocardial ischemia induced-cardiac injury through activation of PTEN/PI3K/AKT signaling [15]. There were many studies had reported that EGCG cloud ameliorate cardiac hypertrophy and brosis [21,22]. In our study, we found that EPI could improve heart function and reduce cardiac brosis in hearts of TAC mice and inhibit AngII-induced α-SMA and COLI/III expression.…”

New insights into the role of the Nrf2 signaling pathway in green tea catechin applications

“…Aging-induced cardiac hypertrophy and fibrosis were studied in rats. EGCG reduced ROS production, MDA, increased SOD, CAT, GPx, GR, and GST activities, ascorbic acid, α-tocopherol and reduced glutathione, improved Nrf2 expression, decreased α-SMA expression, attenuated TGFβ1, TNFα, and NFκB gene and protein expression (Muhammed et al, 2018). Hence, these findings suggested that EGCG can be useful to fight against cardiovascular injuries through Nrf2 pathway.…”

Molecular Rescue of Dyrk1A Overexpression Alterations in Mice with Fontup® Dietary Supplement: Role of Green Tea Catechins

“…Previous results have elucidated the potential antifibrogenic role of green tea catechins, like EGCG, in a CCl 4 -induced fibrotic rat showing an increased serum ALT [25]. They postulated that EGCG are potential therapeutic candidates in antifibrotic therapy [30]. Excessive fibrosis in the extracellular matrix with overactivated myofibroblasts increases myocardial stiffness resulting in myocardial dysfunction.…”